Background and Objectives: Placental vascular lesions are significant histopathological findings that indicate disruptions in uteroplacental and fetoplacental circulations and are associated with adverse pregnancy outcomes such as preeclampsia, intrauterine growth restriction (IUGR), and perinatal morbidity. This study aimed to re-examine the frequency and distribution of placental vascular lesions in placentas submitted for histopathological analysis at our center, based on criteria established by the Amsterdam Placental Workshop Group Consensus Statement. Materials and Methods: In this retrospective study, placental samples examined in the Department of Pathology at Akdeniz University Faculty of Medicine from 2016 to 2019 were analyzed. A total of 571 cases with at least one placental vascular lesion identified on histopathology were included. Hematoxylin–eosin-stained sections from all cases were re-evaluated, and maternal vascular malperfusion (MVM), fetal vascular malperfusion (FVM), and other placental vascular pathologies were assessed according to the Amsterdam consensus criteria. Statistical analyses were performed using IBM SPSS Statistics for Windows, Version 25 (IBM Corp., Armonk, NY, USA). Categorical variables were compared using the chi-square or Fisher’s exact test, while continuous variables were analyzed with the Mann–Whitney U test. Results: MVM and FVM were considered the primary outcomes of the study. MVM was identified in 95.1% of cases, whereas FVM was present in 1.9%. Among individual lesions, chorangiosis (97.2%) and villous/perivillous fibrinoid deposition (88.3%) were the most frequent findings, followed by mucinous cystic degeneration of the umbilical cord (61.5%) and dystrophic calcification (58.1%). Retroplacental hematoma was observed in 38.4% of cases. Although no significant association was found between MVM and placental weight or size, umbilical cord length was significantly shorter in MVM-positive cases (p = 0.032). In contrast, FVM showed significant associations with chorangiosis (p = 0.035) and placentomegaly (p = 0.003). The high frequency of chorangiosis may reflect a compensatory angiogenic response to chronic intrauterine hypoxia, potentially mediated by vascular growth factors, with variable effectiveness depending on the severity of the underlying condition. Conclusions: These findings suggest that placental vascular lesions are not only markers of obstetric complications but also serve as morphological indicators of fetoplacental adaptive responses.
Ünal et al. (2026) studied this question.